Craniofacial malformations with obstructive airway narrowing may lead to sleep apnea. Obstructive sleep apnea in turn will lead to abnormal sleep patterns most notably a decrease in REM (rapid eye movement) sleep as well as deeper stages of non REM sleep. Since growth hormone secretion is most pronounced in deeper sleep stages of non REM sleep, a disordered sleep pattern may lead to a reduction in growth hormone secretion. Moreover, since the bulk of growth hormone in children is released as a sleep related event, craniofacial malformations causing apnea may dampen or even prevent sleep-related growth hormone release. This hypothesis is strongly supported by the noted increased incidence of poor statural growth in children with craniofacial malformations despite adequate caloric intake. It is also possible that patients with craniofacial malformations (e.g. midline defects) have classical growth hormone deficiency. To test this hypothesis we will evaluate patients with craniofacial anomalies for the presence or absence of sleep apnea. Patients with and without sleep apnea will have 24 hour determination of the circadian pattern of plasma hGH. With concomitant polysomnographic recordings patients will be restudied 3 months after surgical correction of the craniofacial anomalies which lead to sleep apnea. The patients will thus serve as their own controls. The purpose of this study is to determine whether obstructive sleep apnea and disordered growth hormone secretion is causally related to the short stature frequently seen in children with craniofacial anomalies. If we can demonstrate a cause-effect relationship between short stature and obstructive sleep apnea caused by craniofacial malformations a new potentially curable factor causing poor growth in children will be identified. Stated succintly, all patients with craniofacial anomalies must be carefully screened for obstructive sleep apnea, a potentially reversible cause of short stature.